Production of experimental tumors by a variety of chemical carcinogens may be inhibited by the administration of butylated hydroxyanisole (BHA), butylated hydroxytoluene (BHT), ethoxyquin, selenium and vitamin E (anticarcinogenic agents). Investigations in these and other laboratories have established that administration of BHA to rodents (1) protects a variety of target tissues against the production of tumors by a wide range of chemical carcinogens, (2) reduces the levels of mutagenic metabolites from benzo(a)pyrene (BP) and numerous therapeutic agents, in vivo (antimutagenic), (3) elevates the hepatic levels of various enzymes involved in the detoxification of reactive metabolite and alters other hepatic enzymes and catalytic constituents (enzyme modifications), (4) increases the concentrations of non-protein thiol compounds in the liver and several other tissues. Utilizing these recently discovered principles and methodologies, we propose to study the biochemical mechanisms involved in the antimutagenic effects of the anticarcinogenic agents as a prerequisite for the design and development of more selective means to reduce or eliminate the mutagenic and carcinogenic potential of environmental chemicals. We shall compare the antimutagenic potencies of anticarcinogenic agents using two defined carcinogens (BP and acetylamino fluorene). The alterations in biochemical parameters caused by anticarcinogenic agents will be correlated also with their antimutagenic effects. Additionally, the production of various metabolites of the carcinogens will be analyzed in biological fluids by high pressure liquid chromatography (HPLC) and the mutagenic activity of these fractions will be determined.